Introduction

Post-traumatic stress disorder (PTSD) is a neurological disorder caused by prolonged exposure to actual or threatened death, serious injuries or sexual violence, followed by specific symptom clusters that last for over one month (Al Jowf et al., 2021). Most people picture PTSD as something that happens to soldiers coming home from war – this picture is not wrong, but it is incomplete. The diagnosis itself, first added to psychiatric manuals back in 1980, was never meant to be limited to adults, and a growing body of research is showing just how much children have been overlooked in this field (Torrico & Mikes, 2024). Putting together twelve systematic reviews and meta-analyses spanning over 121,000 children and adolescents worldwide, the rate of PTSD among trauma-exposed youth is estimated to be 25%, a number that sits close to what is typically reported in combat veterans and considerably higher than the 6-15% range long cited by the National Centre of PTSD (Tamir et al., 2025). When the researchers split their data by application date (older, more than five years), they reported a PTSD rate of 17%, while reviews published within the last five years reported 28%. It is suggested that this jump reflects a mix of better screening, more traumatic exposure globally (including Covid-19) and more rigorous diagnostic methods being used in newer studies (Tamir et al., 2025). Additionally, women, teenagers over 14, those lacking social support, those who felt trapped or powerless during the traumatic event, and those grieving a death were most likely to develop PTSD (Tamir et al., 2025).

PTSD in children is further complicated by the fact that clinicians have been debating whether “one” PTSD really exists or if it splits into different presentations, including a dissociative form (Hansen et al., 2017). The dissociative subtype, characterised by depersonalisation indicated by a child feeling detached from their body, was initially described mainly in adult samples (Hansen et al., 2017; Wolf et al., 2017). This UK study attempted to close that gap by re-analysing data from two existing youth trauma cohorts: one of the cohorts followed roughly 230 children after a single traumatic incident while the other followed about 110 children who had experienced ongoing abuse or neglect (White et al., 2024). Using statistical clustering to sort children into symptom groups, the researchers found the dissociative subtype is significantly more prevalent in children when compared to what has been reported in adults (White et al., 2022).  This subtype followed a similar recovery trajectory to standard PTSD and also served as an early warning sign for PTSD persisting longer term (Wang et al., 2024). Critical dissociation on its own predicted how much a child’s daily functioning was impaired, even after accounting for other trauma-related thinking patterns known to sustain PTSD (White et al., 2024; Vonderlin et al., 2022). In other words, these findings suggest that dissociative symptoms represent a clinically meaningful aspect of PTSD in children and adolescents (Scheeringa et al., 2018).

Subtypes aside, the way PTSD presents itself in a child rarely matches the adult template most people are familiar with. PTSD affects four domains at once: how a child thinks, their mood, their physical sense of self and their behaviour. Because a child’s version of these symptoms does not always resemble an adult’s, cases are routinely missed or mistaken for something else, like ADHD or a mood disorder. Left unrecognised, childhood PTSD often becomes chronic, contributes to developing other psychiatric conditions later in life and raises suicide risk (Torrico & Mikes, 2024). 

Altogether, this points to a clear conclusion: PTSD in children is a scaled-down version of adult PTSD. It shows up more often than older estimates suggested. It splits into subtypes that behave differently in youth than in adults, and it presents through a different set of symptoms than the disorder most people picture. To understand why, this paper will turn to the two tools that dominate research into the neural side of paediatric PTSD: electroencephalography (EEG) and functional magnetic resonance imaging (fMRI). We will first look at what EEG studies have picked up in traumatised children. The electrical moment-to-moment activity patterns have been proposed as candidate markers of the disorder before moving to fMRI research, which instead maps where in the brain that altered activity is happening and how strongly different regions communicate with one another. We will lay out the specific markers researchers have identified, how consistently they show up across studies, and what they might mean for diagnostics or treatment down the line. Then, we will explain common mental conditions that develop because of PTSD development, and what risks are present as a result. This paper sheds light on the antecedents of how the usage of neurobiological markers identifies early childhood PTSD symptoms to prevent the progression of co-morbidities and risks.

Common Co-Morbidities and Risks

Children exposed to traumatic childhood experiences can go on to develop PTSD and, in many cases, undergo a significant shift in their developmental trajectory (Cruz et al., 2022). This trajectory can include the development of co-morbidities, where one or more distinct conditions are present in an individual alongside a primary diagnosis (Xi, 2024, citing Harrison et al., 2021). Children and adolescents with significant early trauma often receive inaccurate or incomplete diagnoses, leading to ineffective treatment, and a substantial proportion of PTSD cases go undiagnosed altogether (Gagnon-Sanschagrin et al., 2022). This diagnostic gap extends to medical co-morbidities as well, leaving both categories underreported and untreated (Cruz et al., 2022). The sections below examine each in turn, starting with psychiatric co-morbidities before turning to the physical toll trauma takes on the body (Cruz et al., 2022).

Substance Abuse

Substance use disorder (SUD) is one of the most consistently documented psychiatric comorbidities of PTSD in youth, with childhood trauma and PTSD both independently raising the risk of early substance use, which in turn predicts more severe SUD later on (Becker et al., 2023). Because PTSD and SUD reinforce each other once both are present, integrated treatment addressing both conditions is necessary (Becker et al., 2023). A neuroimaging-focused review adds a biological layer to this picture, finding that PTSD and SUD share overlapping brain circuitry, including structural and functional changes in limbic regions and the brain’s salience, default-mode and frontoparietal networks, which helps explain why substance use in trauma-exposed adolescents can further entrench trauma-related memory processes rather than simply numbing them (Etami et al., 2023).

Researchers have proposed several explanations for why trauma and substance use track together: the self-medication hypothesis, where PTSD symptoms drive substance use as coping; the susceptibility hypothesis, where substance use itself raises later PTSD risk; and the shared liability hypothesis, where a pre-existing factor raises risk of both (Patel et al., 2024). A nationwide adolescent study found support for self-medication and partial support for shared liability, but not susceptibility (Patel et al., 2024). This tracks with earlier findings that interpersonal violence in particular is associated with especially high rates of PTSD-SUD comorbidity and overlapping symptomatology, reinforcing that this pairing reflects genuine shared vulnerability rather than coincidence (Hinckley & Danielson, 2022).

Dementia

Dementia is not something children with PTSD experience during childhood, but a long-term risk that appears decades later, in adulthood or old age (Xie et al., 2025). A UK Biobank cohort study of more than 145,000 participants found that people who experienced emotional, physical and sexual abuse in childhood carried roughly 2.2, 3.2 and 3.2 times the risk of developing all-cause dementia, respectively, compared to those without such a history, with risk climbing further for people traumatised in both childhood and adulthood (Xie et al., 2025).

This finding is echoed by two independent meta-analyses. One pooled studies of traumatic life events and dementia risk in older adults, finding childhood trauma among the strongest predictors and pointing to reduced hippocampal volume and HPA-axis changes as possible mechanisms (Severs et al., 2023). Another study, which focused specifically on adverse childhood experiences (ACEs), reached the same conclusion (Abouelmagd et al., 2024). A separate neuroimaging study found that psychiatrically healthy adults with a childhood trauma history show measurably “older” brains than their actual age would predict, an accelerated-ageing pattern that appears even without any diagnosed psychiatric condition, suggesting trauma’s biological toll can accumulate in the brain well before symptoms emerge (Hendrikse et al., 2025).

Borderline Personality Disorder

Borderline personality disorder (BPD) is a psychiatric condition marked by unstable moods, an unstable sense of self and unstable relationships, and it is often accompanied by PTSD (Riou et al., 2024). There is a substantial prevalence of trauma history among individuals with BPD, and the clinical, cognitive and cerebral parallels shared between the two conditions, such as overlapping emotional dysregulation and reduced hippocampal volume in both disorders, suggest a trauma-related aetiology for BPD (Riou et al., 2024). Whether this shared profile reflects two independent conditions or PTSD worsening the hippocampal changes already present in BPD remains an open debate; a multi-centre study is now recruiting adolescents with BPD alone, BPD with PTSD, and healthy controls to investigate this directly (Riou et al., 2024).

A 2025 review synthesising 112 neuroimaging studies adds further weight to the trauma-related view, finding that BPD involves consistent disruptions in the prefrontal-amygdala circuit and the brain’s default mode network, the same regions responsible for emotion regulation and self-referential thought, and that these disruptions partially overlap with those seen in PTSD (Giannoulis et al., 2025). Separately, because BPD is less understood in adolescents than in adults, a 2025 study surveyed 1,147 Chinese adolescents and found that among those with five or more BPD features, 64.9% screened positive for dissociative symptoms, PTSD or complex PTSD (C-PTSD), with trauma-related factors explaining 52.9% of the variance in BPD features and 89% reporting a childhood abuse or neglect history, supporting BPD as at least partly a trauma response (Yuan et al., 2025). This is consistent with earlier findings that childhood emotional, sexual and physical abuse significantly predicts later BPD symptoms, while emotional neglect specifically predicts dissociative symptoms (Cheng et al., 2023, citing Sar et al., 2006).

Chronic Pain

Findings have indicated a connection between the long-term and complex impact of adverse childhood events, such as abuse and neglect, on both PTSD and C-PTSD and chronic pain, defined as pain lasting longer than three months, in adulthood (Karimov-Zwienenberg et al., 2024). C-PTSD characterises the long-lasting consequences following exposure to repeated and often inescapable trauma regarding significant relationships, like intimate personal violence and childhood abuse (Karimov-Zwienenberg et al., 2024). It is reported that, while psychological distress has previously been identified as a component of the phenomenon of adverse childhood events contributing to increased risk of chronic pain in adulthood, few studies have explored the role of PTSD in this phenomenon, indicating a gap in research regarding trauma-informed pain management and psychological treatment for comorbid trauma and chronic pain (Karimov-Zwienenberg et al., 2024). Despite this gap, many studies reported that childhood trauma, especially in the form of maltreatment, demonstrated higher prevalence and severity for emotional abuse and neglect compared to other forms of maltreatment. Compared to other medical conditions, studies also found higher childhood maltreatment rates and severity in individuals with chronic pain, particularly towards individuals who had events related to neglect, sexual abuse and emotional abuse, suggesting that chronic pain is connected to childhood trauma more often than other health conditions (Karimov-Zwienenberg et al., 2024). Moreover, some studies found that the most prevalent traumatic events were reported in childhood as opposed to adulthood, the most commonly reported trauma being physical, sexual and emotional abuse (Karimov-Zwienenberg et al., 2024, citing Gardoki-Sauto et al., 2022).

Epilepsy

Epilepsy is a chronic neurological condition that describes a sudden burst of abnormal electrical activity in the brain, causing an individual to experience recurring seizures (National Institute of Neurological Disorders and Stroke, 2025). A complex relation can be drawn between epilepsy and psychological trauma: for one, a longitudinal national study indicated that people with PTSD were four times more likely to have epilepsy than those without PTSD (Ertan et al., 2025). However, on the other hand, epilepsy is a complex chronic disease that can increase the risk of having seizure-related traumatic events such as post-seizure PTSD; for example, some studies show that people with epilepsy are more vulnerable to traumatic experiences such as motor vehicle accidents, assaults and suicides compared to the general population (Ertan et al., 2025).

Neurobiological Markers and Treatment of PTSD in Childhood

MRI and EEG Markers of PTSD

Neurobiological markers, defined as objectively measurable indicators of brain structure, function and electrical activity, are essential for addressing critical gaps in early identification of childhood PTSD (Heyn, 2019). Reliance on subjective behavioural checklists has contributed to misdiagnosis rates approaching 50% as trauma-related symptomatology frequently overlaps with ADHD and ASD (Torrico & Mikes, 2024). Unlike interviews, neurobiological markers provide quantifiable, pre-symptomatic data essential for early PTSD intervention, as delayed treatment risks comorbidity and suicide (Scheeringa, 2018). Therefore, EEG and fMRI represent established neuroimaging modalities for identifying these early symptoms, essential for the prevention of PTSD progression. 

Electroencephalography provides researchers with a way to detect these hidden changes. A child may appear “fine” on the outside while their brain continues to show measurable effects of trauma. By using scalp electrodes to measure real-time electrical activity, EEG captures neural dynamics within millisecond precision. In children exposed to trauma, several patterns were identified that serve as neurobiological markers of trauma-related changes (Berger, 1924).

Among the most studied EEG markers is frontal alpha asymmetry (FAA), which reflects differences in alpha wave activity (8-13Hz) between the left and right frontal regions. In a study of 165 children aged 5-17 years, FAA during resting-state EEG was significantly more negative in the trauma-exposed group, indicating greater left lateralised alpha activity and corresponding avoidance-oriented motivation (Im et al., 2022). The same study also found out that alpha suppression, which is the difference in alpha amplitude between eyes-open and eyes-closed conditions, was marginally greater in the trauma-exposed group. These findings are supported by evidence of reduced resting alpha power in PTSD, which is directly linked to cortical hyperexcitability (Nicholson et al., 2023). Beyond the frontal lobes, temporal-posterior alpha power is also reduced in trauma-exposed adolescents, implicating fear circuitry dysfunction (Marcu et al., 2024). 

Importantly, the effects of childhood adversity are not limited to alpha bands. Further research demonstrated that childhood adversity predicts frontal oscillatory asymmetry across multiple frequency bands, with specific patterns depending on individual symptom profiles (Moran et al., 2017). Another key method is the theta/beta ratio, which represents the balance between slow-wave theta (4-8Hz) and fast-wave beta (13-30Hz) activity. This ratio is elevated in traumatised youth and has been correlated with emotional regulation deficits (Miskovic & Keil, 2012). Moreover, event-related potentials (ERPs) that measure the brain’s electrical response to specific stimuli such as startling sounds or trauma-related images revealed amplified P300 or late positive potential (LPP) responses to threat-related cues that demonstrate hypervigilance (Hedrick et al., 2024).

These EEG markers facilitate early PTSD detection in several critical ways. For instance, hyperarousal patterns such as heightened physiological reactivity when the nervous system remains on high alert can be identified before behavioural symptoms fully develop  (Nicholson et al., 2023). EEG also aids diagnostic differentiation. While ADHD is typically presented with excess theta and low beta activity, PTSD is characterised by frontal asymmetry and exaggerated threat response (Ayaz, 2025). Furthermore, applications of markers allow the tracking of treatment response as normalisation of alpha asymmetry and reduced ERP amplification shows distinct correlations with symptom improvements. 

Functional magnetic resonance imaging measures blood-oxygen-level-dependent (BOLD) signals, which track regional brain activity with high spatial resolution by detecting changes in oxygenated blood flow. In children with PTSD, fMRI has consistently identified abnormalities within frontolimbic circuitry. The network involves the prefrontal cortex (PFC), amygdala and hippocampus, that plays an important role in emotional processing and fear regulation (Wolf & Herringa, 2016).

One of the most crucial findings is amygdala hyperactivation. The amygdala processes fear and detects potential threats; youth with PTSD have demonstrated exaggerated BOLD responses in this region (Herringja, 2018). In a comparative study, youth with PTSD exhibited hyperactivation of the dorsal anterior cingulate cortex (dACC) in response to threat-related images, a pattern that is consistent with abnormal heightened fear responses (Wolf & Herringa, 2016). Divergent developmental trends are also observed through age-related analyses. While healthy youth demonstrate decreased amygdala activation with age, those with PTSD show increased activation over time, suggesting a process of developmental sensitisation (Keding & Herringa, 2016). Correspondingly, prefrontal cortex activation shows opposite age-related patterns that positively predict dorsomedial PFC activation in healthy youth, but negatively predicts in those with PTSD.

Structural MRI analyses further revealed additional vulnerabilities. Youth with PTSD show decreased ventromedial PFC volume, as well as an age-related decline in hippocampal volume that presents itself as a neurotoxic process (Keding & Herringa, 2015). On a functional level, resting state fMRI identified increased connectivity within the default mode network, alongside greater anticorrelation between the default mode and attentional control networks in youth with PTSD (Patriat et al., 2016).  Critically, these fMRI-detected abnormalities, particularly amygdala hyperactivation and reduced PFC-amygdala connectivity, can be identified prior to formal diagnosis. This early detection enables intervention at a stage when the developing brain remains mostly plastic (Zhutovsky et al., 2021). Without fMRI, these early neural signatures would remain undetectable, delaying intervention until symptoms have already consolidated into chronic and disabling conditions.

Neuroplasticity and Treatment of PTSD in Children

There is a critical window during the first 1000 days of a child’s life in which the foundations of typical and atypical development of the brain are established (Dan, 2025). This is the period when the rate of growth of the brain reaches its peak, reaching approximately 80% of its adult size (Dan, 2025). These early years of the immature brain are also identified as the most crucial in shaping the child’s ability to learn and comprehend life around them. Their experiences in this period can significantly alter their mindsets and lives in the future (First Things First, 2018). Unlike an adult brain, which is less ‘plastic’ and harder for their neural pathways to adapt (Pace, 2020), a child’s brain is much more malleable, providing an important basis for early interventions aimed at reworking cognitive, emotional and behavioural patterns. 

One method of early intervention introduces trauma-focused cognitive behavioural therapy (TF-CBT), which is an evidence-based intervention for cases where the child has been exposed to trauma, or exhibits trauma-related mental health symptoms (Cohen, Berliner & Mannarino, 2010). This psychological treatment focuses on identifying and modifying maladaptive patterns (Lukianoff & Haidt, 2011), using various methods such as exposure therapy and cognitive-behavioural principles to treat symptoms (de Arellano et al., 2014). The aim of TF-CBT is to educate the child about their trauma, developing strategies to reduce the negative responses linked with the experience while ensuring the child is able to modulate the strong emotions and thoughts linked with their trauma (de Arellano et al., 2014). This method utilises the broader concept of neuroplasticity, which is the ability for the neurons and neural networks in the brain to modify their behaviour and patterns in response to different environments and experiences (Dan, 2019). By using behavioural and cognitive mechanisms to alter neural networks, it allows children, whose neural connections are easier to modify, to revise maladaptive thought patterns and portray more positive associations to any stimuli that may be linked to the trauma. Research reveals that TF-CBT can reduce symptoms of PTSD in youth, decreasing post-traumatic stress syndrome (PTSS) and disturbances in self-organisation (DSO) (Jensen et al., 2022). There are, however, individual cases in which patients have not responded to or have discontinued treatment. Understanding that treatment should be based on the severity of symptoms rather than the trauma type can greatly improve results of TF-CBT (Jensen et al., 2022). 

These treatments and their success rates hence raise a question: if neuroplasticity allows the brain to heal, does that mean trauma scars are temporary? The act of changing our neural networks helps reduce pain and changes how we respond to memories, allowing for trauma scars to not be strictly permanent (Henley, 2025). So while neuroplasticity and TF-CBT do not completely erase trauma scars, it is still tremendously helpful in the recovery process, enabling many children to reshape their lives away from their past trauma.

Discussion

The evidence synthesis provided indicates that childhood PTSD is substantially more prevalent than previously known, with the recent meta-analyses demonstrating prevalence rates of 28% among traumatised children, which substantially exceeds previously reported estimates of approximately 6-15% (Tamir et al., 2025). The neurobiological markers discovered via EEG and fMRI studies include frontal alpha asymmetry, an elevated theta/beta ratio, increased ERP reactivity to threat, amygdala hyperactivity, reduced hippocampal volume and disrupted PFC-amygdala interaction. Collectively, these findings suggest that quantifiable biomarkers for brain abnormalities can be detected before behavioural symptoms are exhibited (Im et al., 2022; Wolf & Herringa, 2016; Hedrick et al., 2024). These markers address critical diagnostic gaps because of the high misdiagnosis rate of almost 50% associated with the difficulty of distinguishing PTSD symptoms from those of ADHD, mood disorders and ASD (Torrico & Mikes, 2024). 

From the results, it is apparent that neurobiological markers form the biological foundations that may contribute to the trajectory of psychiatric and neurological comorbidities. Dysregulation of the stress system and frontal asymmetry associated with paediatric PTSD may increase vulnerability to substance use according to the theory of self-medication (Patel et al., 2024). Findings from fMRI concerning reduced hippocampal volume and altered patterns of brain ageing may indicate potential pathways through which childhood trauma is associated with increased risks of cognitive decline, such as dementia, later in life (Xie et al., 2025). Neurobiological similarity between BPD and PTSD points to the common trauma-induced aetiology (Riou et al., 2024), and the reciprocal association of PTSD and epilepsy highlights the importance of early identification and intervention (Ertan et al., 2025). High neuroplasticity of the paediatric brain accounts for the success of trauma-focused cognitive behavioural therapy (Cohen et al., 2010). Neurobiological markers offer a unique chance to improve the treatment process through objective monitoring of the treatment response (Nicholson et al., 2023). 

Integration of neurobiological markers in the assessment of paediatric PTSD could facilitate earlier identification and potentially reduce the risk of chronic PTSD and associated comorbidities, such as substance use disorder, dementia, chronic pain, BPD and epilepsy. This strategy may improve people’s well-being, lower medical costs and alleviate significant public health burdens related to childhood traumatic experiences. Moreover, personalised approaches to treatment may be developed due to the objective observation of the patient’s treatment response. 

However, several limitations should be considered. The development of standardised procedures and normative values at different developmental stages is essential before the implementation of neurobiological approaches in clinics (Scheeringa, 2018). High costs and low availability of fMRI limit its practical application, while the relatively lower resolution and potential data interference of EEGs may risk accuracy in diagnoses (Blocka & Yetman, 2021). Furthermore, the neurobiological factors linking childhood PTSD and late-life dementia and epilepsy over extended periods of time are not fully revealed (Zwienenberg et al., 2024). Future research in this field should focus on longitudinal study designs that follow the development of children who experience traumatic experiences from early identification through adulthood, identifying how neurobiological markers predict the development of specific comorbidities and differential treatment outcomes. 

The current evidence supports the potential value of utilising neurobiological markers in paediatric PTSD screening strategies, thereby promoting a shift from a reactive to a proactive approach to clinical practice. EEG and fMRI contribute to more timely diagnosis, earlier intervention and objective evaluation of treatment response. Proper allocation of resources into early detection through neurobiological markers and evidence-based interventions, such as TF-CBT, could improve long-term outcomes for children suffering from traumatic experiences.

Conclusion

Childhood PTSD is more common, more consequential and more biologically embedded than earlier estimates suggested. This paper has shown that the disorder rarely presents in isolation: substance abuse, dementia, borderline personality disorder, chronic pain and epilepsy all share a documented, trauma-linked relationship with PTSD, whether through overlapping brain circuitry, shared stress-response dysregulation or common origins in childhood adversity. What ties these threads together is neurobiology. EEG and fMRI markers, including frontal alpha asymmetry, elevated theta/beta ratios, amygdala hyperactivation, and reduced hippocampal and prefrontal connectivity, reveal that trauma leaves a measurable signature in the brain well before behavioural symptoms fully emerge, offering a path past the near-50% misdiagnosis rate that has long obscured paediatric PTSD from view. Crucially, the same developing brain that makes children vulnerable to these lasting changes also makes them unusually responsive to intervention: the high neuroplasticity documented in early childhood is precisely what allows treatments like TF-CBT to meaningfully reshape trauma-driven neural patterns. Taken together, this evidence points toward a clear shift in how paediatric PTSD should be approached: not as a single behavioural diagnosis to be treated reactively, but as a neurobiological process that, identified early enough, can be met with equally early, targeted and effective intervention.

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